Institute for Cell and Molecular Biosciences, Newcastle University, Campus for Ageing and Vitality, Newcastle upon Tyne NE4 5PL, UK.
Institute of Cellular Medicine, Newcastle University, Campus for Ageing and Vitality, Newcastle upon Tyne NE4 5PL, UK.
Free Radic Biol Med. 2019 Feb 20;132:11-18. doi: 10.1016/j.freeradbiomed.2018.09.013. Epub 2018 Sep 13.
The decline in the musculoskeletal system with age is driven at the cellular level by random molecular damage. Cells possess mechanisms to repair or remove damage and many of the pathways involved in this response are regulated by redox signals. However, with ageing there is an increase in oxidative stress which can lead to chronic inflammation and disruption of redox signalling pathways. The complexity of the processes involved has led to the use of computational modelling to help increase our understanding of the system, test hypotheses and make testable predictions. This paper will give a brief background of the biological systems that have been modelled, an introduction to computational modelling, a review of models that involve redox-related mechanisms that are applicable to musculoskeletal ageing, and finally a discussion of the future potential for modelling in this field.
随着年龄的增长,骨骼肌肉系统的衰退在细胞层面上是由随机的分子损伤驱动的。细胞拥有修复或清除损伤的机制,许多参与这一反应的途径都受到氧化还原信号的调节。然而,随着年龄的增长,氧化应激会增加,从而导致慢性炎症和氧化还原信号通路的破坏。所涉及的过程的复杂性导致了使用计算模型来帮助提高我们对系统的理解、检验假设和做出可测试的预测。本文将简要介绍已建模的生物系统、计算模型的介绍、综述适用于骨骼肌肉老化的与氧化还原相关机制的模型,最后讨论该领域建模的未来潜力。